Hepcidin in acute iron toxicity

Am J Emerg Med. 2009 Sep;27(7):761-4. doi: 10.1016/j.ajem.2008.06.003.

Abstract

Background: Hepcidin regulates extracellular iron concentration by inhibiting iron release from macrophages and preventing iron absorption in the intestine. Our objective was to evaluate the expression of hepcidin in the liver in acute iron poisoning in a rat model.

Methods: Male Wistar rats were assigned to group 1, who received 750 mg/kg elemental iron (LD(50)) by gavage, and group 2 (control), who received distilled water. Iron concentrations and liver transaminases were measured in the serum. Hepcidin messenger RNA levels were measured in the liver.

Results: Mean serum iron levels, aspartate aminotransferase, alanine aminotransferase, and uric acid were significantly higher in group 1 compared to group 2 (P < .0001, P = .01, P < .0001, and P = 0.0001, respectively). Hepcidin messenger RNA levels in the liver were significantly higher in the study group (P = .005).

Conclusions: In acute iron intoxication, hepcidin expression in the liver significantly increased. Further studies are needed to determine whether hepcidin levels correlate with the severity of the intoxication.

MeSH terms

  • Acute Disease
  • Alanine Transaminase / blood
  • Animals
  • Antimicrobial Cationic Peptides / metabolism*
  • Aspartate Aminotransferases / blood
  • Disease Models, Animal
  • Hepcidins
  • Intestinal Absorption / drug effects*
  • Iron / poisoning*
  • Kidney / metabolism
  • Liver / metabolism*
  • Male
  • RNA, Messenger / analysis
  • Rats
  • Rats, Wistar
  • Uric Acid / blood

Substances

  • Antimicrobial Cationic Peptides
  • Hamp protein, rat
  • Hepcidins
  • RNA, Messenger
  • Uric Acid
  • Iron
  • Aspartate Aminotransferases
  • Alanine Transaminase